Tumor promoting properties of a cigarette smoke prevalent polycyclic aromatic hydrocarbon as indicated by the inhibition of gap junctional intercellular communication via phosphatidylcholine-specific phospholipase C.

Tumor promoting properties of a cigarette smoke prevalent polycyclic aromatic hydrocarbon as indicated by the inhibition of gap junctional intercellular communication via phosphatidylcholine-specific phospholipase C.

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http://www.wikidata.org/entity/Q34505307

Q34505307

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Structure-activity-dependent regulation of cell communication by perfluorinated fatty acids using in vivo and in vitro model systems Effects of the lifestyle habits in breast cancer transcriptional regulation Interplay between smoking-induced genotoxicity and altered signaling in pancreatic carcinogenesis Phosphatidylcholine Specific PLC-Induced Dysregulation of Gap Junctions, a Robust Cellular Response to Environmental Toxicants, and Prevention by Resveratrol in a Rat Liver Cell Model Serum metabolomics analysis reveals impaired lipid metabolism in rats after oral exposure to benzo(a)pyrene Bronchoalveolar Lavage Fluid Utilized Ex Vivo to Validate In Vivo Findings: Inhibition of Gap Junction Activity in Lung Tumor Promotion is Toll-Like Receptor 4-Dependent "Bad Luck Mutations": DNA Mutations Are not the Whole Answer to Understanding Cancer Risk.Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression.Polycyclic aromatic hydrocarbon-induced signaling events relevant to inflammation and tumorigenesis in lung cells are dependent on molecular structure.The loss of cellular junctions in epithelial lung cells induced by cigarette smoke is attenuated by corilagin Impact of obesity on 7,12-dimethylbenz[a]anthracene-induced altered ovarian connexin gap junction proteins in female mice Modulation by aspirin and naproxen of nucleotide alterations and tumors in the lung of mice exposed to environmental cigarette smoke since birth Activation of group IVC phospholipase A(2) by polycyclic aromatic hydrocarbons induces apoptosis of human coronary artery endothelial cells Evolution of Microbial Quorum Sensing to Human Global Quorum Sensing: An Insight into How Gap Junctional Intercellular Communication Might Be Linked to the Global Metabolic Disease Crisis.Gap junctional intercellular communication as a target for liver toxicity and carcinogenicity.Secondhand Smoke-Prevalent Polycyclic Aromatic Hydrocarbon Binary Mixture-Induced Specific Mitogenic and Pro-inflammatory Cell Signaling Events in Lung Epithelial Cells.Methoxychlor and Vinclozolin Induce Rapid Changes in Intercellular and Intracellular Signaling in Liver Progenitor Cells.Chloral hydrate decreases gap junction communication in rat liver epithelial cells.Global gene expression changes in human embryonic lung fibroblasts induced by organic extracts from respirable air particles.Environmentally prevalent polycyclic aromatic hydrocarbons can elicit co-carcinogenic properties in an in vitro murine lung epithelial cell model.

P2860

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P2860

Tumor promoting properties of a cigarette smoke prevalent polycyclic aromatic hydrocarbon as indicated by the inhibition of gap junctional intercellular communication via phosphatidylcholine-specific phospholipase C.

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http://www.wikidata.org/entity/Q34505307

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